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THE EYE EXAMINATION: Appendix

(as part of the Head and Neck Examination)
Introduction to Clinical Medicine (ICM) II

I. USEFUL OPHTHALMOLOGY ATLAS WEB-SITES

q http://www.eyeatlas.com/

q http://www.nyee.edu/page_deliv.html?page_no=50

q http://webeye.ophth.uiowa.edu

II. OVERVIEW of the EYE EXAMINATION

A. General Vision:
1. Visual acuity (use a pocketsize near vision test card at the bedside and measure
distance vision with a wall mounted Snellen chart [if available]).
2. Visual field testing by confrontation (or perform later as part of the Neurological
examination)
B. External examination: eyebrows, eyelids, lashes, conjunctiva (scleral & palpebral
conjunctiva), cornea, and anterior chamber
C. Pupillary size, shape, and reactions (e.g., “pupils equal, round, reactive to light &
accommodation” = PERRLA: cranial nerves II and III, and sympathetic innervation of
the eye)
D. Ocular motility (e.g., “extra-ocular motion intact” = EOMI: cranial nerves III, IV, and
VI)
E. Direct ophthalmoscopy (red reflex, optic cup/disc, retinal blood vessels, retinal
background, and macula)

III. OPHTHALMOLOGICAL EXAMINATION – DETAILS

A. GENERAL VISION
1. Examination
q Visual acuity
q Visual fields

2. Details
a. Measure Visual Acuity:
Use a “pocket visual screener” card at an appropriate distance (14 inches
usually), testing each eye individually and then both eyes together. If
available, distance vision should likewise be tested with a wall mounted
Snellen chart.
b. Assess Visual Fields via Confrontation:
Remember to check the visual quadrants (superior & inferior temporal,
superior & inferior nasal) of each eye separately. Visual pathways are
complicated, but very useful: consult a visual pathway “map” to help
interpret findings.

3. “Pearls”
• Visual acuity is the “vital sign” of the eye examination.

• Visual fields: assessing the field defect, if present, is very helpful in

localizing the lesion. Neurological lesions usually respect the vertical
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midline of the patient’s vision and affect both eyes (even though the
lesion is unilateral). Prechiasmal field defects (from an optic nerve or
actual ocular process) are usually unilateral. Optic nerve lesions often
respect the horizontal midline.
ü A monocular defect lies anterior to the optic chiasm and is a problem
of either the optic nerve or the retina on the involved side.
ü Bitemporal hemianopia: (i.e., the temporal fields of both eyes are
“cut”) typically occurs secondary to a craniopharyngioma in children
or a pituitary tumor in adults.
ü Homonymous hemianopia (i.e., visual field on the same side of each
eye is “cut”): generally reflects a lesion of the contralateral cerebral
cortex.

B. EXTERNAL EXAMINATION
1. Examination
q Eyebrows
q Eyelids
q Lashes
q Conjunctiva (scleral & palpebral conjunctiva)
q Cornea
q Anterior Chamber

2. Details
a. Use a penlight
b. Examine in a systematic fashion
c. Gently retract the lower lid to inspect the palpebral conjunctiva

3. “Pearls”
• External hordeolum (sty): a tender pustule on the eyelid margin.
• Internal hordeolum (chalazion): a tender nodule/pustule deep to the eyelid
margin.
• Ectropion: outward turning of the eyelid margin.
• Entropion: inward turning of the eyelid margin.
• Pinquecula: small, rounded, yellowish collection of elastic fibers on the
conjunctiva that suggests repeated and prolonged exposure to sunlight.
• Pterygium: similar to pinquecula—including its cause---but the growth
extends from the conjunctiva onto the cornea.
• Scleral icterus: a serum bilirubin of ≥ 3 mg/dL is usually required to see
scleral icterus (jaundice).
• Palpebral conjunctival pallor: loss of the reddish hue of the distal palpebral
conjunctiva (just inside the lid margin) correlates with a hematocrit in the low
20’s or less.
• Chemosis: edema of the bulbar conjunctiva.

C. PUPILLARY EXAMINATION
1. Examination
q Assess the iris of both eyes
q Note size and shape of each pupil
q Assess pupillary light reflex (both direct and consensual)
2. Details
Pupillary Responses:
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The “swinging flashlight test” assesses CN II, CN III (this latter carries
parasympathetic fibers to the sphincter pupillae and constricts the pupil), and
sympathetic nerve innervation of the dilator pupillae muscle.

Technique: the room should be dimly lit. Use a pen light shone from below and
up into the “normal” (e.g., the right) eye: that eye should undergo a brisk
constrictive response to the “direct” light and an identical “consensual” response
should simultaneously occur in the left eye. Now, quickly swing the penlight over
to the left eye from below. If the left and right eyes are normal, then both pupils
should constrict to a similar degree whether the “swinging” penlight is shone in
the right or the left eyes. In other words, the direct and the consensual
responses should be the same if the afferent pathways in both eyes are the
same.

If there is a relative afferent pupillary defect of, for example, the left eye (a
Marcus Gunn pupil—explained further below), the direct response in the left eye
will be weaker than the consensual response was in the normal right eye. The
pupils of both eyes will be seen to dilate as the penlight is swung from the normal
right eye to the abnormal left eye. Swing the penlight back again into the normal
right eye: the left pupil will consensually constrict again as the right pupil
constricts to the direct light.

3. “Pearls”
• You will frequently see small rhythmic variations in the pupil size depending
on the degree of light, as pupillary adjustment takes place. This is called
hippus, and it is normal. Don’t confuse hippus with an afferent pupillary
defect.

• The parasympathetic nervous system (which constricts the pupil and arrives
at the eye via CN III) and the sympathetic nervous system (which dilates the
pupil and does not arrive at the eye via CN III) determine pupillary size. The
sympathetic nervous system reaches the dilator pupillae muscle in the
anterior part of the eye via a complicated route:
ü First-order fibers descend from the ipsilateral hypothalamus -- brainstem
-- cervical spinal cord to T1 -T2, where they synapse with ipsilateral
preganglionic sympathetic fibers.
ü The second-order preganglionic sympathetic fibers exit the thoracic
spinal cord via a ventral root and ascend the cervical chain to synapse in
the superior cervical ganglion.
ü Third-order postganglionic neurons leave the superior cervical ganglion
and travel along the carotid artery as the carotid sympathetic plexus.
They reach the dilator muscle of the iris via the long ciliary nerves, the
sympathetic root of the ciliary gangion and short ciliary nerves, and the
nasociliary nerve. (Reminder: the nasociliary nerve is a branch of the
ophthalmic nerve (V1 branch of CN V).

• Abnormal pupillary shape may occur as a consequence of:

ü Cataract excision (resulting in an irregular, sometimes pear-shaped
pupillary contour)
ü Blunt trauma (traumatic mydriasis; or, if trauma was severe enough,
tears in the iris)
ü Past iritis (resulting in adhesions [synechiae] of the iris to the anterior
capsule of the lens)
ü Coloboma of the iris (a congenital defect that results in a “keyhole”
shaped pupil)
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• Some causes of unequal pupils include:

ü Physiological anisocoria (may occur as a normal variant in up to 20% of
the population)
ü Pharmacological dilation
ü Horner’s syndrome (ptosis, miosis, anhydrosis): may occur secondary to
a lesion of the sympathetic trunk in the neck: for example, tumors,
trauma, apical pulmonary disease, tabes dorsalis, syringomyelia, or
neuritis. The ptosis happens because one of the two muscles that raise
the eyelid (the superior tarsal muscle) is a smooth muscle innervated by
the sympathetic nervous system. (The principal elevator eyelid muscle
[levator palpebrae superioris] is a striated muscle and innervated by CN
III).
ü Third nerve palsy (resulting in mydriasis)
ü Other causes of asymmetrical pupils include acute iritis, acute angle
closure glaucoma, and old trauma.

• On accommodation (near vision or convergence) the pupils should constrict.

When the patient looks far away again, the pupils should dilate. If the
patient’s pupils are equal, round, and both are reactive to light normally, then
there is no need to also check for accommodation—it will be present.

• Argyll Robertson pupils are small, irregular pupils that react poorly or not at
all to light (either directly or consensually), but they do constrict appropriately
with accommodation (this is termed “light-near” dissociation). Its classic
cause is tertiary syphilis, but other etiologies include diabetes and Wernicke’s
encephalopathy.

• Adie’s pupil is an irregularly dilated pupil that exhibits minimal or no reaction

to light, slow constriction to accommodation, and slow redilatation after
accommodation. An Adie’s pupil is usually unilateral, mydriatic, somewhat
oval, and benign (it is most often found in young women). With pilocarpine
stimulation (0.125%), there is a hyper-miotic response of the Adie’s pupil as
compared to the other side.

• Marcus Gunn pupil (relative afferent pupillary defect) results from an

abnormal afferent pathway with a normal efferent pathway. The pupil of the
involved eye constricts (although poorly) with direct light stimulus, but when
the penlight shines in the opposite normal eye, the pupil of the affected eye
now constricts appropriately. When the penlight is then shined back into the
affected eye, the pupil of the affected eye dilates. A classic cause of a
Marcus Gunn pupil is optic neuritis, but other severe retinal processes (e.g.,
retinal detachment) may also cause this worrisome abnormality.

D. OCULAR MOTILITY
1. Examination
q Carefully assess the movements of both eyes (assessing cranial nerves III, IV,
and VI and the extra-ocular muscles innervated by those nerves)

2. Details
a. The Oculomotor nerve (III) carries parasympathetic fibers that result in
constriction of the pupil. In addition, it supplies all but two of the extrinsic muscles
of the eye. It also supplies the levator palpebrae superioris muscle, which is the
principal muscle responsible for raising the eyelid.
b. The Trochlear nerve (IV) supplies the superior oblique muscle. This muscle
moves the adducted eye downward.
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c. The Abducens nerve (VI) supplies the lateral rectus muscle. This muscle moves
the eye laterally (resulting in abduction).

When testing the above nerves and muscles, have the patient hold their head still
while they look at your finger. Be sure to position your finger far enough in front
of the patient so they see your finger in all directions of gaze. Move your finger
slowly (physicians have a tendency to rush and move their finger too rapidly for
the patient to adequately follow the movements). The pattern to trace with your
finger is the “classic H” described below (the example presented here shows the
movements, CN's, & muscles involved for the patient’s left eye):

Up

Inferior Oblique III Superior Rectus III

Medial Lateral

Medial Rectus III Lateral Rectus VI

Superior Oblique IV Inferior Rectus III

Down
3. “Pearls”
• Dysfunction of one or more of these CN’s, or the muscles they innervate, will
cause diplopia (double vision).

• As noted above, a third nerve palsy will result in mydriasis. If third nerve
function is further compromised, the eye on the involved side will deviate
laterally because of unopposed [CN VI] lateral rectus muscle strength [and a
weak medial rectus secondary to the CN III dysfunction]).

• Strabismus is ocular misalignment secondary to a weakness or a paralysis of

one or more extra-ocular muscles. A –tropia is a manifest strabismus and a
–phoria is a latent strabismus. The direction of the strabismus is indicated
by the appropriate prefix: exo- is a horizontal deviation outwards (divergent),
eso- is a horizontal deviation inwards (convergent), hypo- is a vertical
deviation downwards, and hyper- is a vertical deviation upwards. For
example, esotropia is a manifest, convergent strabismus and exophoria is a
latent, divergent strabismus.

E. OPHTHALMOSCOPY (Fundoscopy)
1. Examination
q Use the ophthalmoscope to evaluate the red reflex, optic disc/cup, retinal blood
vessels, retinal background, and macula.

2. Details
a. Dim the lights in the room (if possible); if dilation drops are to be used,
tropicamide (1%) is a reasonable drug choice (duration of dilation approximately
6 hr).
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b. Have the patient gaze at a distant “target” (e.g., an object on a counter, a

doorknob, a light switch) to help minimize accommodation.
c. Adjust your ophthalmoscope beam and brightness (a small beam of light is better
for smaller pupils).
d. Begin with a neutral diopter (focus on your hand), and begin your view 15
degrees lateral to the patient’s visual axis.
e. Place your “free” hand on the patient’s forehead, and gently use your thumb to
help raise their upper lid. The patient’s glasses should be removed (but they can
still wear contact lenses). If you wear glasses, those also should be removed.
Use your right eye to look in the patient’s right eye; use your left eye to look in
the patient’s left eye.
f. Start about 1 foot away from the patient and first assess their red reflex.
g. After obtaining the red reflex, slowly close in on your patient still staying 15
degrees off of their visual axis, until your forehead is nearly or actually touching
your own hand on their forehead. As you move in, focus your scope to correct
for refractive errors of the patient and yourself. You should be coming in on their
optic disc at 15 degrees off of their visual axis (which is also the “blind spot” in
their vision).
h. Carefully examine the following parts of the retina:
ü The disc, the cup, and the cup to disc ratio
ü The arteries and veins radiating out from the optic cup
ü Other retinal lesions in the retinal “background”
ü Finally, the macula (which is two optic disc diameters temporal to the
patient’s optic disc). The macula is a deeper red color than the other parts of
the retina, and in younger people you may notice a bright foveal light reflex.
It is uncomfortable for the patient to have you look at their macula, so do this
part of the examination last and quickly.

3. “Pearls”
• A cataract is an opacity of the lens. It will show up as a darkened silhouette
within the red reflex.

• Leukocoria indicates a total loss of the red reflex. In children it is concerning

and usually reflects a serious underlying problem (including retinoblastoma).

• The optic disc (or nerve head) is that point where the axons of the retinal
ganglion cells form the optic nerve. The optic cup is the whitish central
“excavation” of the disc (and it is the site where the retinal vessels enter and
exit the eye).

• The normal cup to disc ratio should be < 1:2 (usually < 1:3). An optic cup ≥
50% of the total disc diameter is suspicious for glaucoma. An optic cup ≥
70% of the diameter of the disc strongly suggests glaucoma.

• Retinal Changes in Hypertension (these are classically described in Medicine

texts, although ophthalmologists do not spend a lot of time trying to identify
each of the earlier stages):
1. Vasoconstrictive phase: earliest change; not probably seen by us non-
ophthalmologist mere mortals.
2. Sclerotic phase: arteriolar narrowing, AV nicking (note: AV nicking is
permanent once it occurs, even if the hypertension is brought under
control), and alteration of the light reflex. Moderately sclerosed arterioles
look like copper wires. Severely sclerosed vessels look like silver
wires. Complications of the sclerotic phase may include central retinal
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artery occlusion, branch retinal artery occlusion, central retinal vein

occlusion, and branch retinal vein occlusion.
3. Exudative phase: flame hemorrhages, “hard” exudates (yellowish/whitish
well-demarcated retinal lesions secondary to damaged and leaky blood
vessel walls), and cotton-wool spots (these are nerve fiber layer infarcts
[NFL infarcts]: they are white, indistinct, opaque areas).
4. In malignant hypertension, the exudative phase of retinal vascular
changes occurs concomitantly with optic disc swelling (papilledema).

• Retinal Changes in Diabetes Mellitus:

1. Non-proliferative diabetic retinopathy (NPDR): depending on severity,
this can include dot -and-blot hemorrhages, microaneurysms, exudates,
and cotton-wool spots (NFL infarcts).
2. Pre-proliferative phase: intraretinal microvascular abnormalities or dilated
capillaries that are very permeable and venous irregularities (venous
beading).
3. Proliferative retinopthy: growth of fine tufts of new blood vessels and
fibrous tissue from the inner retinal surface or optic nerve head.
4. Macular edema (localized swelling or thickening of the macula, often
associated with exudates in the macula).